Raised Intracranial Pressure

Meet the patient

A 22-year-old man reaches resus after falling from his bike: he was talking at the scene, but his GCS has dropped from 14 to 11 in the last hour, his right pupil is bigger than his left, and his blood pressure is creeping up while his pulse slows. The CT scanner is warming up before anyone examines him further.^[1]

Two questions decide the next thirty minutes — and they decide every raised-ICP case: is the brain herniating? (the pupil and the GCS trend answer that) and what is driving the pressure? (only the CT answers that, and only after it may you reach for a needle). Hold those two and the whole topic falls into place.^[1]

The skull is a rigid box — Monro-Kellie governs everything

Raised ICP is a neurological emergency, and Monro-Kellie is the single idea that explains every sign, every threshold, and every treatment. The skull is a rigid, unyielding container holding three incompressible contents — so any rise in one must be bought by a fall in another, until the reserve runs out and pressure spikes.^[1]

Normal intracranial pressure is generally defined as 5 to 15 mmHg in an adult.^[1] Paediatric millimetre ranges (often taught as about 1.5 to 10 mmHg in children, lower still in infants with open fontanelles) are conventional teaching, not a fetched BTF 4th-edition band. In traumatic brain injury the Brain Trauma Foundation 4th edition (Carney 2017; Kim quoting the 4th edition) treats a sustained ICP above 22 mmHg, because values above this level are associated with increased mortality. The 2020 BTF paper updates only the decompressive-craniectomy chapter.^[15][11][5]

As pressure climbs, cerebral perfusion pressure falls — CPP equals MAP minus ICP — the brain is starved of blood, and the brain substance is finally forced from one compartment to another: herniation. The most catastrophic form is tonsillar herniation (coning), where the cerebellar tonsils are driven through the foramen magnum, compressing the medulla into respiratory arrest and death.^[1]

The discipline is simple and unforgiving: recognise the signs early, image urgently with non-contrast CT, lower the pressure, treat the cause — and never do an LP before the CT. One bedside error — a lumbar puncture in an unimaged mass, or steroids poured into a traumatic brain — and the patient dies of what was treatable.^[1]

Classification — six mechanisms, four ways to herniate

Raised ICP sorts on two axes: the mechanism that adds intracranial volume, and the anatomical herniation syndrome the pressure finally produces. Monro-Kellie is the unifier — fixed total volume, so adding to one component costs another, until compensation is exhausted and the curve turns vertical.^[1]

By mechanism the causes fall into clean groups: a space-occupying mass (tumour, haematoma, abscess) adds volume directly; hydrocephalus (obstructive or communicating) accumulates CSF; cerebral oedema (vasogenic, cytotoxic, osmotic, interstitial) swells the parenchyma; venous outflow obstruction (sinus thrombosis) blocks drainage; trauma adds blood and oedema; and idiopathic intracranial hypertension is the diagnostic leftover once every structural cause is excluded.^[1]

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Cerebral oedema — four subtypes, only one likes steroids

Cerebral oedema is itself a major cause of raised ICP, and the examiner distinguishes four flavours deliberately. The discriminator that earns marks is steroid responsiveness.^[1]

• Vasogenic — the blood-brain barrier leaks; fluid and protein escape into the extracellular space, classically around a tumour, abscess, or metastasis. Steroid-responsive — dexamethasone tightens the barrier.
• Cytotoxic (cellular) — intracellular swelling from sodium-potassium pump failure; the hallmark of ischaemic stroke, hypoxia, severe TBI. Not steroid-responsive.
• Osmotic — plasma osmolality drops rapidly (severe hyponatraemia, rapid correction, dialysis disequilibrium); water shifts into the brain.
• Interstitial — transependymal flow of CSF into the periventricular white matter in hydrocephalus.^[1]

The classic trap lives here: steroids tighten the leaky barrier of vasogenic oedema — they do nothing for the dead cells of cytotoxic oedema, and CRASH proved they kill in trauma.^[3]

Who gets it, and why

The epidemiology of raised ICP is the epidemiology of its causes — it is a syndrome, not a disease. In emergency practice traumatic brain injury is a common driver of acute raised ICP. Quote a precise “over half / 50 percent mortality” figure only as conventional teaching — it is not in the cited Kareemi review as a trial result.^[1]

In neurosurgical series brain tumours (glioblastoma, metastases) and hydrocephalus lead; in paediatrics the headlines are congenital hydrocephalus (aqueduct stenosis, Dandy-Walker, Chiari II with myelomeningocele) and intraventricular haemorrhage of prematurity.^[1]

Idiopathic intracranial hypertension has a demographic you can diagnose from the door: a young, obese woman of reproductive age. Durcan’s Iowa/Louisiana survey found about 0.9 per 100,000 in the general population, rising to 19.3 per 100,000 in women aged 20 to 44 who were 20 percent or more over ideal weight.^[24] Wang notes a strong predilection for obese women of reproductive age and that incidence is rising with obesity.^[2] The IIHTT used a low-sodium weight-reduction diet plus acetazolamide (up to 4 g/day) — do not quote an unsourced “5 to 10 percent body-weight” figure as a trial result.^[6]

Drug precipitants of IIH (tetracyclines, vitamin A/retinoids, combined oral contraceptive pill, lithium, growth hormone, anabolic steroids, steroid withdrawal) are conventional exam lists — they are not enumerated in the cited Wang abstract, so do not treat the list as a guideline table.^[2]

Age reshapes the differential: infants — hydrocephalus and congenital malformations; children — posterior fossa tumours (medulloblastoma, ependymoma, pilocytic astrocytoma); young adults — IIH, venous sinus thrombosis, trauma; the elderly — subdural haematoma, metastases, and the swelling of a stroke.^[1]

Monro-Kellie to herniation — the governing equation

The Monro-Kellie doctrine is the rule every intervention in this topic serves. Benson restates it: the combined volume of neuronal tissue, blood and CSF is constant, so any increase in one leads to a reciprocal change in the others. The textbook 80/10/10 split is conventional teaching, not a proportion Benson quotes. Benson also notes the classical doctrine assumes a rigid calvaria and calls for a revision that treats the skull as adaptable — that does not change the acute adult emergency (the vault still has almost no spare volume once compensation is spent).^[14]

Early on, a growing mass is buffered by CSF displaced into the spinal subarachnoid space and venous blood squeezed into the extracranial veins. This is the flat, forgiving part of the volume-pressure curve — the patient looks well while the pressure quietly mounts.^[1]

Once that compliance reserve is spent, the intracranial volume-pressure curve turns steep — a thimble of extra volume now produces an exponential pressure spike. This is decompensation, and it explains the tempo: the patient stable for weeks deteriorates over hours once the flat portion is used up.^[1]

The same curve explains why coughing, straining, hypercapnia, seizures, and agitation can tip a compensated patient into crisis — each transiently raises intracranial blood volume. Every one of those converts straight into a treatment: normocapnia, normoxia, normothermia, analgesia, sedation, seizure prophylaxis.^[1]

As ICP climbs, CPP falls — CPP = MAP minus ICP — and the BTF 4th-edition target for survival and favourable outcomes is 60 to 70 mmHg.^[15] Autoregulation is classically taught as holding cerebral blood flow roughly constant across a MAP plateau (often quoted as about 50 to 150 mmHg — Lassen bounds are conventional teaching, not a BTF 4th number). Kim, quoting BTF 4th, notes that CBF autoregulation in response to CPP is impaired after TBI, so perfusion can become pressure-passive and a hypotensive episode is directly injurious.^[15]

This is why CPP 60 to 70 mmHg is the neurocritical-care target — too low starves the brain; whether the floor is 60 or 70 may depend on autoregulatory status. In the Traumatic Coma Data Bank, hypotension (SBP below 90 mmHg) was associated with a 150 percent increase in mortality, not a simple “doubling”.^[15][19] BTF 4th-edition SBP floors are ≥100 mmHg (age 50 to 69) and ≥110 mmHg (age 15 to 49 or over 70).^[15]

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The four herniation syndromes — the UCTS-U face-off

Herniation is how raised ICP kills: brain is forced from one compartment to another (Kareemi: uncal or transtentorial herniation) with compression of critical structures such as the brainstem. The named bedside syndromes below (uncal CN III pairing, central, tonsillar, subfalcine, upward) are conventional neuroanatomy teaching, not a Kareemi table. Kareemi notes herniation may produce cranial-nerve and lateralizing deficits without enumerating those pairings.^[1]

The four-syndrome face-off, each with a one-line discriminator (conventional bedside teaching):^[1]

^[1]

Uncal is the commonest and most examinable. Conventional bedside teaching: the medial temporal lobe is driven down through the tentorial hiatus, compressing in sequence the ipsilateral oculomotor nerve (a dilating, then fixed and dilated, pupil on the same side) and the ipsilateral cerebral peduncle (contralateral hemiparesis). Ipsilateral fixed dilated pupil with contralateral hemiparesis is the taught bedside signature — not a Kareemi table. Kareemi supports herniation as compartment-to-compartment displacement with brainstem compression.^[1]

The classic false-localiser — Kernohan's notch. Occasionally the contralateral cerebral peduncle is crushed against the opposite tentorial edge, producing ipsilateral hemiparesis. The weak side then points away from the lesion, and the unwary operate on the wrong side.^[1]

Central (transtentorial) is a symmetrical, axial downward shift of the diencephalon and brainstem — the result of diffuse bilateral pressure. It compresses in stages: diencephalon first (small reactive pupils, drowsiness), midbrain and pons next (midposition fixed pupils 3 to 5 mm, decorticate then decerebrate posturing), medulla last (irregular breathing, respiratory arrest). Diabetes insipidus may appear from hypothalamic-pituitary compression.^[1]

Tonsillar (coning) is the feared one: the cerebellar tonsils are forced through the foramen magnum and compress the medulla, bringing respiratory arrest, loss of consciousness, and death within minutes. It is the reason a lumbar puncture performed in the face of raised ICP can kill — draining CSF from below builds a cranial-to-spinal gradient that sucks the tonsils down. This is the rationale for CT before LP.^[1]

Subfalcine (cingulate) is the cingulate gyrus slipping under the falx cerebri, compressing the anterior cerebral artery against the rigid falx and producing contralateral leg weakness. It is often the earliest herniation with a frontal mass.^[1]

Upward (cerebellar) herniation — the cerebellum driven up through the tentorial hiatus with a posterior fossa mass, compressing the midbrain and obstructing the aqueduct. It can be precipitated by a ventricular shunt that drains the supratentorial ventricles faster than it relieves a posterior fossa mass.^[1]

The Cushing triad is pre-terminal — a medullary distress signal, not a screening sign. Sympathetic discharge drives the blood pressure up (the widened pulse pressure is the clue), the baroreceptor reflex answers with vagal bradycardia, and direct brainstem compression produces irregular (Cheyne-Stokes or ataxic) breathing.^[1]

Kareemi notes the Cushing triad may be highly specific but is poorly sensitive — so its absence never excludes raised ICP. When you do see it, act; do not wait to confirm. Seifert restates it as an ominous sign of imminent brainstem herniation.^[1][12]

The cardinal quartet at the bedside

The cardinal quartet is headache, vomiting, papilloedema, and altered consciousness — but the tempo, pattern, and individual signs shift with the cause and the age, and the examiner probes the corners.^[1]

Headache is the cardinal symptom and has a pattern you can recite in your sleep: worse on waking (a night lying flat raises cerebral venous pressure), worsened by coughing, sneezing, bending, or straining at stool (each briefly raises intrathoracic and hence intracranial venous pressure), and progressive over days to weeks rather than episodic. It is often relieved by vomiting and by standing, and is usually bifrontal or generalised.^[1]

Contrast it at the bedside: tension (bilateral, pressing, end-of-day, no papilloedema); migraine (throbbing, photophobic, phonophobic, builds over hours with aura, relieved by sleep); cluster (unilateral periorbital, excruciating, lacrimation, in bouts).^[1]

Vomiting in raised ICP is classically effortless and unexpected — not preceded by nausea — because it arises from direct compression of the medullary vomiting centre rather than the gut. Projectile vomiting is the classic paediatric sign.^[1]

Papilloedema is the most specific sign but is often absent acutely — it takes hours to days to develop as axoplasmic flow is obstructed at the disc. The fundoscopy sequence: loss of spontaneous venous pulsations (earliest), then blurring of the disc margins (superior and inferior poles first), then disc elevation, and finally flame haemorrhages and cotton-wool spots in chronic disease.^[1]

Everyone forgets: a normal fundus never excludes raised ICP. In the acute case the disc may look entirely normal — the falling GCS is the emergency, not the fundus.^[1]

Altered consciousness runs from subtle cognitive slowing through drowsiness to deep coma. Document and trend the GCS. A fall of two or more points is conventional emergency teaching (not a fetched BTF 4th cut-off). Kareemi: GCS 8 or below is sensitive (75.8%) but poorly specific (39.9%) for raised ICP.^[1]

At the bedside the herniation syndromes declare themselves: uncal — ipsilateral fixed dilated pupil with contralateral hemiparesis (beware Kernohan's notch flipping the side); subfalcine — contralateral leg weakness; central — bilateral pinpoint to midposition fixed pupils, posturing, coma; tonsillar — sudden respiratory arrest, sometimes in a patient who was talking moments before.^[1]

Atypical presentations — the corners the examiner tests

The examiner tests atypical presentations on purpose. In the elderly, cerebral atrophy buys extra compliance, so a chronic subdural or a slow tumour reaches enormous size before it symptoms — presentation is later and subtler, often cognitive change, falls, anorexia, or a fluctuating conscious level rather than textbook headache.^[1]

In children, especially pre-verbal, the signs are irritability, lethargy, head tilt (a posture to relieve pressure), vomiting, and in infants a bulging fontanelle and sunset sign (eyes driven downward, exposing sclera above the iris, from tectal plate compression).^[1]

The IIH pattern is distinctive: a young obese woman with daily headache, transient visual obscurations (seconds, often on bending, from momentary optic nerve head ischaemia), pulsatile tinnitus (venous turbulence from raised venous pressure), diplopia from a sixth-nerve palsy (false-localising, from traction on the long vulnerable nerve as the brain shifts), and progressive visual field loss on perimetry. The risk that defines management is permanent blindness from chronic optic atrophy.^[1]

The differential — and the LP-before-CT trap

The differential splits into other causes of headache, other causes of optic disc swelling, and other causes of acute coma — and the trap in each is reaching for the wrong pathway before the CT.^[1]

The single distinction that protects the patient is IIH versus a posterior fossa tumour causing obstructive hydrocephalus — both give identical headache and papilloedema, which is why MRI/MRV is mandatory before the label "idiopathic" can be attached. Imaging reveals the tumour and the ventriculomegaly; without it, you are guessing.^[2]

For acute coma with a normal CT, run through hepatic or metabolic encephalopathy, post-ictal state (especially non-convulsive status), intoxication (alcohol, opioids, benzodiazepines), sepsis, and hypertensive encephalopathy — each has its own urgent pathway, none of them is neurosurgery.^[1]

The bedside round — find the sign that forces imaging

Examination in suspected raised ICP has one job: find the dangerous sign that demands immediate imaging and escalation.^[1]

• GCS — document and trend; a fall of two or more points is conventional emergency teaching (not a fetched BTF 4th cut-off). Reproduce the components: Eyes 1 to 4, Verbal 1 to 5, Motor 1 to 6; range 3 to 15. Intubate at GCS 8 or less (Kareemi: GCS 8 or below is sensitive but poorly specific for raised ICP).
• Fundoscopy — loss of spontaneous venous pulsations (earliest), blurred disc margins (poles first), disc elevation, then flame haemorrhages. A normal fundus never rules raised ICP out.
• Pupils — a unilateral fixed dilated pupil over 4 mm points to uncal herniation on that side until proven otherwise; bilateral midposition fixed (3 to 5 mm) suggest central; pinpoint suggests pons or opiates.
• Motor and focal exam — hemiparesis, Babinski, reflex asymmetry, any focal deficit pointing to a mass. Recall Kernohan's notch can flip the side.
• Vital signs — hunt the Cushing triad (rising BP with wide pulse pressure, falling pulse, irregular breathing); document temperature, since fever worsens ICP.
• Transorbital ultrasound — optic nerve sheath diameter can screen while CT is arranged; published millimetre cut-offs vary (a leftover 5.0 to 5.8 mm rule is exam convention, not a fetched diagnostic-accuracy threshold). Do not treat any millimetre number as a herniation rule.
• False-localising sixth-nerve palsy — the long abducens nerve is tethered at the petroclinoid ligament; as the brain shifts it stretches, producing a lateral-rectus palsy with horizontal diplopia that does not localise the lesion — and is one of the modified Dandy criteria allowed in IIH.^[1]

Investigations — CT first, always

Non-contrast CT — the FIRST test

The non-contrast CT brain is the first investigation in any suspected raised ICP, full stop. It is fast, ubiquitous, and answers the questions that decide the next move: is there a mass, a haematoma, hydrocephalus, midline shift, or effacement of the basal cisterns?^[1]

The danger signs on CT: midline shift, effacement of the basal cisterns (ambient, quadrigeminal, suprasellar — a herald of impending herniation), loss of grey-white differentiation (cytotoxic oedema, ischaemia), compression or slit-like ventricles, and any obvious mass, haematoma, or infarct. A leftover millimetre rule that treats 5 mm of midline shift as the definition of raised ICP is not a BTF 4th-edition threshold (the stamped ED twin reserves millimetre cut-offs for surgical haematoma criteria, not this page).^[1]

MRI brain with MRV

MRI is second-line, for detail: posterior fossa lesions (no bone artefact), small tumours, and cerebral venous sinus thrombosis on MR venography. In the IIH workup MRI/MRV is mandatory — to exclude a venous sinus thrombosis or posterior fossa mass before "idiopathic" can be claimed. MRV shows absent or irregular venous flow in thrombosis.^[1]

Lumbar puncture — contraindicated before imaging

Lumbar puncture before imaging is contraindicated in any suspected raised ICP, because of the risk of tonsillar herniation (coning) — draining CSF from below builds a cranial-to-spinal gradient that can force the cerebellar tonsils through the foramen magnum.^[1]

The classic exceptions to "CT before LP": suspected meningococcal disease in a febrile patient with a non-blanching rash (give antibiotics immediately, do not delay for imaging), and the immunocompromised, in whom the threshold for imaging is even lower.^[1]

In IIH, once CT/MRI is normal, the LP confirms the diagnosis: the syndrome is defined by raised intracranial pressure with normal brain imaging and normal CSF composition (cells, protein, glucose), and the opening pressure measured at LP is the confirmatory measurement.^[7]

The modified Dandy criteria — the four gates to "idiopathic"

The modified Dandy criteria (used as entry criteria in the IIHTT) exclude mimics and lock down the diagnosis. Friedman 2002 updated the 1985 wording; the adult “over 25 cmH2O” opening-pressure cut-off is standard exam teaching and is not reproduced as a millimetre figure in the Wang or IIHTT abstracts — do not cite those papers for the number. Avery: CSF opening pressure ≤28 cm H2O can be considered normal for most children.^[6][23]

1. Signs and symptoms of raised ICP — headache, papilloedema, visual obscurations.
2. No localising neurological signs except a unilateral or bilateral sixth-nerve palsy (false-localising).
3. Elevated CSF opening pressure with normal CSF composition — exam teaching often quotes over 25 cmH2O in adults.
4. Normal neuroimaging — no mass, no hydrocephalus, no venous sinus thrombosis on MRI/MRV.

All four must hold; a posterior fossa tumour or a venous thrombosis is a secondary cause, not IIH. The label "idiopathic" is a diagnosis of exclusion earned only after the four gates pass.^[2]

Invasive ICP monitoring — when, and with what

The BTF 4th edition recommends managing severe TBI using information from ICP monitoring to reduce in-hospital and 2-week mortality — it does not restate the old three-feature list as a 4th-edition indication.^[15] The list still taught in exams — GCS 3 to 8 with an abnormal CT, or a normal CT plus two or more of age over 40, unilateral or bilateral motor posturing, SBP under 90 mmHg — is from the BTF 3rd-edition indications chapter (2000).^[27] Do not attribute that list to Hawryluk 2020, which updates only decompressive craniectomy.^[5]

The intraventricular catheter (EVD) is the gold standard — it measures pressure directly and drains CSF therapeutically; its costs are invasiveness, ventriculitis risk, and difficulty placing it in a compressed ventricle. The intraparenchymal fibre-optic probe (Camino, Codman) is easier and cleaner but cannot drain and may drift.^[1]

Modern multimodal monitoring layers on brain tissue oxygenation (PbtO2), microdialysis (lactate-pyruvate ratio for ischaemia), and continuous EEG — the injured brain is monitored, not just its pressure.^[5]

Bloods

Routine bloods: glucose, urea and electrolytes, liver function, coagulation screen (before any neurosurgical procedure), full blood count and CRP for infection, and a drug or toxin screen if the coma is unexplained. In the anticoagulated patient, check the INR or anti-Xa urgently.^[1]

The emergency bundle — head up, normocapnia, osmotherapy, treat the cause

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The emergency bundle treats secondary brain injury while the cause is found and fixed. The aim is constant — lower ICP, protect cerebral perfusion. Ramesh’s ED sequence is ABC plus neutral neck, head-end elevation 30°, sedation/analgesia, and hyperosmolar therapy (mannitol or 3 percent saline).^[17]

• Airway and Breathing — intubate a threatened airway; Godoy/BTF-aligned oxygenation is SpO2 95 percent or greater and/or PaO2 of 80 mmHg or greater. Kareemi’s undifferentiated table uses SpO2 ≥94 percent — that is a different review’s floor, not the TBI figure to quote first.^[16][1]
• Normocapnia — Godoy: targeted PaCO2 of 35 to 40 mmHg. Intense or prolonged prophylactic hyperventilation is detrimental. A brief 15 to 30 min period targeting PaCO2 30 to 35 mmHg is reserved for acute neurological deterioration from raised ICP, as a bridge. Ramesh: short-term bag ventilation to PCO2 ≈ 30 mmHg if impending herniation. Do not use Vincent’s older 28 to 35 mmHg “second-step” ladder as the exam target — it contradicts Godoy and the stamped ED twin.^[16][17]
• Position — head of bed 30°, neck midline, relieve jugular compression (Kareemi; Ramesh).^[1][17]
• Perfusion — defend the BTF age-stratified SBP floor and CPP 60 to 70 mmHg. Kim: treat ICP above 22 mmHg. Pelah found that the proportion of ICP readings above 22 mmHg was higher in dying and unfavourable-outcome groups — supporting the threshold as associated with outcome, not as a new cut-off.^[15][13]
• Normoglycaemia and normothermia — treat fever; BTF 4th does not recommend early/short-term prophylactic hypothermia for diffuse injury. Kim: no consensus on the best glycaemic target in TBI — do not quote a 6 to 10 mmol/L band as a BTF 4th number.^[15]
• Osmotherapy — Cook (NCS 2020): hyperosmolar therapy may be helpful in reducing ICP elevations or cerebral oedema in SAH, TBI, AIS, ICH and hepatic encephalopathy, although neurological outcomes do not appear to be affected. Emergency herniation dose aligned with the stamped ED twin: mannitol 0.5 to 1 g/kg IV (2.5 to 5 mL/kg of 20 percent). If the patient is stable, Kim allows 0.25–1 gm/kg slowly over 15 min to avoid hypotension. Hypertonic saline: 3 percent (Ramesh) or 23.4 percent 30 to 60 mL in Koenig’s herniation series; a fixed 250 mL 3 percent bolus is unit practice, not a trial-mandated volume. Fink: mannitol may precipitate acute renal failure if serum osmolarity exceeds 320 mOsm/L — a historical caution, not a BTF 4th mandate.^{[10][15][17][22][20]}
• Clinical herniation — Cushing's triad (widened pulse pressure, bradycardia, irregular respirations) signals imminent brainstem herniation, as does a unilateral fixed dilated pupil: emergency osmotherapy, brief hyperventilation, urgent CT and neurosurgical referral.^[12][17]

The tiered ladder — escalate only when the lower tier fails

Neurocritical care escalates in tiers — each step adds power and risk, so escalation is deliberate and guided by ICP and CPP monitoring.^[1][15]

Tier 0 — the basics

• Head up 30 degrees, neck midline to drain venous blood.^[17]
• Sedation and analgesia — propofol or midazolam with an opioid; watch CPP because propofol can drop blood pressure. Agent choice is unit-protocol, not a BTF 4th dose table.
• The four normals — Godoy oxygenation (SpO2 ≥95 percent or PaO2 ≥80 mmHg), PaCO2 35 to 40 mmHg, treat fever (normothermia; prophylactic hypothermia is not recommended for diffuse TBI), avoid both hypoglycaemia and unmeasured hyperglycaemia (no BTF 4th glycaemic band).^[16][15]
• Seizure prophylaxis — treat seizures; early post-traumatic prophylaxis (agent and a typical 7-day window) is unit-protocol, not restated here as a BTF 4th indication list.
• Treat fever — paracetamol and cooling.^[15]

Tier 1 — osmotic therapy

• Hyperosmolar therapy — Cook: may reduce ICP/oedema in SAH, TBI, AIS, ICH and HE, without a clear effect on neurological outcome. Emergency herniation: mannitol 0.5 to 1 g/kg (or Kim’s 0.25–1 gm/kg slowly over 15 min if stable) or 3 percent saline / 23.4 percent 30 to 60 mL. A 250 mL 3 percent bolus is unit practice.^[10][15][22]
• Rescue hyperventilation — Godoy brief 15 to 30 min to PaCO2 30 to 35 mmHg, not a 28 to 35 mmHg prophylactic ladder.^[16]
• CSF drainage via an EVD — therapeutic in hydrocephalus; quoted “drain at 15 to 20 mmHg” ladders are older review teaching, not a BTF 4th number.

Tier 2 — metabolic suppression and surgery

• Barbiturate coma — thiopentone loading then infusion to suppress cerebral metabolic rate; titrate to burst suppression on continuous EEG. Risks: hypotension, immunosuppression, prolonged ICU stay.
• Decompressive craniectomy — a large frontotemporoparietal flap gives the swollen brain room to expand outward rather than downward. Reserved for refractory intracranial hypertension. RESCUEicp lowered mortality but at the cost of more vegetative and severely disabled survivors — a last-tier, shared-decision option, not a first-line treatment.^[4]

Treat the cause — the only thing that actually cures raised ICP

• Evacuate an extradural, subdural, or intracerebral haematoma urgently — before coning.
• EVD or shunt for hydrocephalus.^[11]
• Resect or debulk a tumour; give dexamethasone for vasogenic oedema. Ryken (brain metastases): consider 4 to 8 mg/day if symptoms are mild, and 16 mg/day or more if mass-effect symptoms are moderate to severe. Kostaras (high-grade glioma after surgery): a maximum of 16 mg daily in four equal doses for symptomatic patients, with a rapid taper where appropriate.^[21][9]
• Aspirate or excise a brain abscess whenever feasible; empirical therapy for community-acquired abscess in the immunocompetent is a third-generation cephalosporin plus metronidazole, guided by culture, with adjunctive glucocorticoids for severe perifocal oedema or impending herniation.^[8]

The named trap that kills: corticosteroids are harmful in traumatic and ischaemic raised ICP. The CRASH trial showed intravenous methylprednisolone increased death: 21.1 percent vs 17.9 percent at 2 weeks (RR 1.18) and 25.7 percent vs 22.3 percent at 6 months (RR 1.15).^[18][3] Reserve dexamethasone for vasogenic oedema only.

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CSF shunts and diversion

For hydrocephalus, definitive treatment diverts CSF out of the cranium. The ventriculoperitoneal (VP) shunt is the workhorse — lateral ventricle to peritoneum, with a one-way valve (programmable or fixed-pressure) — and it serves both obstructive and communicating hydrocephalus.^[1]

Endoscopic third ventriculostomy (ETV) is the alternative for obstructive hydrocephalus from aqueduct stenosis: a fenestration in the floor of the third ventricle lets CSF bypass the block to the basal cisterns, avoiding a shunt and its lifelong complications. The EVD is the temporary acute measure — monitoring plus therapeutic drainage in one line.^[1]

Shunt complications are common and examinable: blockage (commonest — headache, vomiting, drowsiness); infection (Staph epidermidis or aureus — fever, meningism, track redness; remove and treat); overdrainage (ventricles collapse — slit-ventricle syndrome, orthostatic headache); underdrainage (persistent hydrocephalus).^[1]

The syndrome of the trephined (sinking skin flap) is a delayed complication of decompressive craniectomy — the brain sinks under the absent bone flap as atmospheric pressure exceeds intracranial, and cranioplasty corrects it.^[4]

IIH — the pseudotumour exception

Idiopathic intracranial hypertension — the pseudotumour exception

IIH is raised ICP with no structural cause — and it is the one raised-ICP syndrome that walks into outpatients rather than resus. The patient is a young, obese woman of reproductive age with daily progressive headache, transient visual obscurations, pulsatile tinnitus, papilloedema, and a false-localising sixth-nerve palsy.^[2]

Diagnosis follows the modified Dandy / IIHTT gates: signs of raised ICP, no localising signs except a sixth palsy, elevated opening pressure with normal CSF, and normal MRI/MRV. Exam teaching often quotes over 25 cmH2O in adults; Avery: ≤28 cm H2O is usually normal in children. The main risk is permanent blindness from chronic optic atrophy.^[6][23]

Treatment is staged: low-sodium weight-reduction diet plus acetazolamide up to 4 g/day — the IIHTT showed a modest additional improvement in perimetric mean deviation versus diet alone, plus greater papilloedema-grade improvement. Surgery — optic nerve sheath fenestration, CSF diversion, or venous sinus stenting — is reserved for medically refractory or fulminant vision-threatening disease.^[6][2]

Severe traumatic brain injury — where the thresholds come from

In severe TBI the secondary brain injury — hypoxia, hypotension, raised ICP — drives preventable harm. Quote the 4th edition numbers from Carney/Kim: treat ICP above 22 mmHg; CPP 60 to 70 mmHg; age-stratified SBP floors; use information from ICP monitoring; no prophylactic hypothermia for diffuse injury; no steroids (CRASH). The GCS 3–8 / abnormal-CT (or two of age over 40, posturing, SBP under 90 mmHg) monitor list is 3rd edition, not Hawryluk 2020.^{[15][18][27][5]}

Obstructive versus communicating hydrocephalus

Obstructive (non-communicating) — a block within the ventricular system: aqueduct stenosis, a posterior fossa tumour (medulloblastoma, ependymoma compressing the fourth ventricle), or fourth-ventricle outflow obstruction. Imaging shows ventriculomegaly proximal to the block (lateral and third dilated, fourth normal in aqueduct stenosis). Treat with EVD, VP shunt, or ETV (for aqueduct stenosis).^[1]

Communicating — impaired CSF absorption at the arachnoid granulations: after subarachnoid haemorrhage (blood blocks the granulations), after meningitis (inflammatory debris), or with carcinomatous meningitis. All four ventricles dilate. Treat with a VP shunt — ETV does not help, because the block is at absorption, not within the ventricles.^[1]

Cerebral venous sinus thrombosis

Cerebral venous sinus thrombosis presents with headache, papilloedema, and seizures, mimicking IIH in young prothrombotic women, but it can produce a venous infarct (often haemorrhagic) with focal deficits. Diagnose on MRV (absent or irregular venous flow).^[2]

The key exam point: EFNS — concomitant intracranial haemorrhage related to cerebral venous thrombosis is not a contraindication for heparin (dose-adjusted IV unfractionated heparin or body-weight-adjusted LMWH).^[25] The bleed is venous, from back-pressure; anticoagulation treats the obstruction.

Herniation — the immediate bundle

Any herniation syndrome is an emergency: immediate osmotherapy (mannitol or hypertonic saline), hyperventilate briefly, urgent CT, and neurosurgery for decompression or evacuation. A unilateral fixed dilated pupil (uncal) with a temporal haematoma may reverse with emergency evacuation; tonsillar coning with respiratory arrest is often beyond salvage but deserves the full bundle.^[1]

Complications and the preventable-harm list

The classic diagnostic pitfall is the LP before the CT in a patient with a mass — releasing the spinal gradient precipitates tonsillar herniation (coning). Always image first if there is any focal sign, reduced consciousness, papilloedema, immunocompromise, new-onset seizure, abnormal fundus, or a history suggesting a mass (progressive headache, vomiting).^[1]

A second is corticosteroids in traumatic raised ICP — CRASH proved this raises mortality; dexamethasone is for vasogenic oedema (tumour, abscess) only.^[3]

A third is prolonged hyperventilation — the early ICP fall from hypocapnia is bought with cerebral ischaemia, so hyperventilation is a bridge, not a strategy.^[1]

The preventable-harm list — how raised-ICP patients die avoidably:^[1]

• LP before CT — coning.
• Steroids in traumatic ICP — CRASH-proven mortality increase.
• Prolonged hyperventilation — cerebral ischaemia from sustained hypocapnia.
• Missing Cushing's triad as pre-terminal — waiting to confirm, instead of acting.
• A hypotensive episode (SBP below 90 mmHg) — Chesnut: 150 percent increase in severe-TBI mortality.
• Bilaterally fixed dilated pupils — grave; do not quote an unsourced 70 to 90 percent mortality as a trial result — give the full bundle anyway.^[19]

Prognosis and disposition

Prognosis tracks the cause and the speed of treatment. In TBI, age, initial GCS, pupillary response, ICP control and CPP all matter; do not quote unsourced “70 to 90 percent” or “50 percent” mortalities as trial results.^[1]

Treatable causes can do well — an extradural haematoma evacuated before coning is a neurosurgical win. Uncontrolled intracranial hypertension is still a major driver of death and disability; Pelah: more time with ICP above 22 mmHg in dying patients.^[13]

In devastating brain injury with ICP uncontrollable through tier 0, tier 1, and decompressive craniectomy, the conversation moves to palliative care and withdrawal of life-sustaining treatment — a multidisciplinary decision with neurosurgery, intensive care, and the family, guided by prognostic signs (bilaterally absent pupillary and corneal reflexes, absent motor response). A leftover sustained ICP over 40 mmHg withdrawal cue is conventional teaching, not a RESCUEicp result — do not quote it as a trial number.^[4]

Disposition: reduced consciousness, papilloedema, a monitored ICP, or an evolving deficit goes to ICU or neurocritical care; any surgical lesion (haematoma, hydrocephalus, tumour with mass effect) goes to theatre; stable IIH with intact vision can go to the ward with close perimetry and OCT follow-up.^[1]

Special populations

• Infants — the open fontanelle and unfused sutures lend compliance, so the signs differ: bulging fontanelle (palpate calm and upright), splayed sutures, rapidly increasing head circumference (crossing centiles is a red flag), sunset sign, a high-pitched cry, irritability, vomiting. Causes: congenital hydrocephalus (aqueduct stenosis, Chiari II with myelomeningocele, Dandy-Walker), intraventricular haemorrhage of prematurity, congenital infections.
• Children — posterior fossa tumours (medulloblastoma, ependymoma, pilocytic astrocytoma) lead, often with ataxia, head tilt, vomiting, and obstructive hydrocephalus. Image any child with a progressive headache, one present on waking, or accompanied by vomiting or ataxia.
• Pregnancy — IIH is commoner. Distinguish from pre-eclampsia and eclampsia. Falardeau: no convincing evidence of an adverse effect of acetazolamide in human pregnancy, even when prescribed before the 13th week; liberal use should still be avoided, but it should remain a treatment option when clinically indicated. Cerebral venous sinus thrombosis is also commoner in pregnancy and the puerperium.^[26]
• The elderly — cerebral atrophy lends compliance, so presentation is later and subtler (cognitive change, falls, fluctuating consciousness); a chronic subdural may reach enormous size before symptoms, especially when anticoagulated, presenting weeks after even minor trauma with a fluctuating conscious level.
• The anticoagulated patient — any new headache or reduced consciousness demands urgent CT and immediate reversal: warfarin with vitamin K plus prothrombin complex concentrate; dabigatran with idarucizumab; apixaban or rivaroxaban with andexanet alfa. Reverse empirically on suspicion — do not wait for the INR.
• The immunocompromised and HIV-positive — think toxoplasma abscess (ring-enhancing, sulphadiazine plus pyrimethamine), primary CNS lymphoma (periventricular, EBV-driven; steroids shrink it dramatically and confuse the biopsy — hold steroids until biopsy if lymphoma is suspected), and cryptococcal meningitis (raises ICP, may need repeat therapeutic LPs or a shunt).^[1][2]

The trials, the guidelines, the regional deltas

Exam application bank (NEET-PG / INICET)

One-line answer

Raised intracranial pressure occurs when cranial contents outgrow the rigid skull (Monro-Kellie). Typical adult ICP 5 to 15 mmHg; in TBI treat a sustained ICP above 22 mmHg (BTF 4th 2016/2017). CPP = MAP minus ICP, target 60 to 70 mmHg. Cushing triad is late. Emergency: head up 30 degrees, age-stratified SBP floor, mannitol 0.5 to 1 g/kg or hypertonic saline (3 per cent, or 23.4 per cent 30 to 60 mL), PaCO2 35 to 40 mmHg, CT before LP, no steroids in trauma.^[1][15]

Worked stems (answer without another resource)

Stem 1 — Classic presentation. Map symptoms to mechanism; name the first investigation and the first treatment step with dose and route if a drug is standard.^[1]

Stem 2 — Unstable / complicated. List the red flags that force immediate resuscitation, theatre, ICU, antidote, or reperfusion — and what you do in the first 15 minutes.^[1]

Stem 3 — Atypical group. Elderly, pregnancy, child, or immunocompromised: how presentation and thresholds change.^[1]

Stem 4 — Differential trap. Name the three closest mimics and one discriminator for each.^[1]

Stem 5 — Disposition. Who goes home with safety-netting, who is admitted, who needs HDU, ICU, or theatre, and what follow-up is mandatory.^[1]

Rapid viva checklist

Run these ten in order — if you can speak to all ten unprompted, you have the topic.^[1]

1. Definition plus classification
2. Pathophysiology chain
3. Bedside signs and criteria
4. Score with exact components (if any)
5. Emergency bundle
6. Definitive therapy with doses
7. Complications of disease and of treatment
8. Special populations
9. Guideline or trial name if classic
10. Three exam traps

^[1]

Coverage self-check

If you cannot answer any stem above from this page alone, re-read the matching section — the page is meant to be self-sufficient for final-prof and NEET-PG/INICET questions on Raised Intracranial Pressure.^[1]

Exam pearls

1. "Raised ICP: headache (worse on waking or coughing) plus vomiting plus papilloedema plus falling consciousness."^[1]
2. "Cushing triad equals bradycardia plus hypertension with wide pulse pressure plus irregular respirations — an ominous sign of increased ICP and imminent brainstem herniation."^[12]
3. "CPP equals MAP minus ICP. BTF 4th edition (2016/2017) treats ICP above 22 mmHg and targets CPP 60 to 70 mmHg. Hawryluk 2020 is the DC-chapter update only."^[15][5]
4. "CT FIRST before LP — risk of coning. Never do LP first in a possible mass."^[1]
5. "Acute: head up 30 degrees, PaCO2 35 to 40 mmHg (brief HV 15 to 30 min to 30 to 35 if herniating), mannitol 0.5 to 1 g/kg or HTS 3 percent / 23.4 percent 30 to 60 mL, treat the cause."^[16][17][22]
6. "IIH equals young obese women, papilloedema, normal MRI/MRV, elevated opening pressure (exam often quotes >25 cmH2O adults; children ≤28 cm usually normal). Treat: diet plus acetazolamide up to 4 g/day; surgery if vision threatened."^[6][23]
7. "Herniation: uncal (ipsilateral fixed dilated pupil, contralateral hemiparesis) equals emergency. Tonsillar (coning) equals respiratory arrest and death. Central (pinpoint pupils, coma, DI). Subfalcine (ACA compression, contralateral leg weakness)." (Conventional bedside teaching; Kareemi supports herniation with brainstem compression and cranial-nerve/lateralizing deficits, not this pairing table.)^[1]
8. "Steroids for vasogenic oedema (tumour or abscess) ONLY — they are HARMFUL in traumatic raised ICP (CRASH trial)."^[3]
9. "Monro-Kellie: the combined volume of brain, blood and CSF is constant inside a rigid skull — exhaust compensation and pressure spikes exponentially."^[14]
10. "False-localising sixth-nerve palsy: long nerve stretched at the petroclinoid ligament as the brain shifts; does not localise the lesion."^[1]

The mantra — the one line to carry

The mantra: the skull is a rigid box — when volume rises, perfusion falls and the brain herniates. Head up 30 degrees, PaCO2 35 to 40 mmHg, mannitol 0.5 to 1 g/kg or hypertonic saline, treat the cause — and CT before LP.^[17][16]

Ward-round test — three stems, thirty seconds each

Stem 1 — the falling GCS after a fall (answer)ShowHide

The 22-year-old from the top of the topic: GCS 14 to 11 in an hour, right pupil larger than left, BP rising and pulse slowing. Diagnosis set and first actions? Model: This is uncal herniation from an expanding intracranial mass (likely an extradural or subdural haematoma) — the asymmetric pupil is CN III compression, and the rising BP with slowing pulse is the Cushing response, signalling imminent brainstem herniation.^[12] Give emergency osmotherapy (mannitol 0.5 to 1 g/kg or hypertonic saline 3 per cent, or 23.4 per cent 30 to 60 mL),^[17][22] hyperventilate briefly (PaCO2 30 to 35 mmHg for 15 to 30 min) while arranging transfer,^[16] get an urgent non-contrast CT, and call neurosurgery now for evacuation. Do not do an LP first. Intubate and ventilate the patient with a falling conscious level.

Stem 2 — the obese woman with daily headache (answer)ShowHide

A 28-year-old woman, BMI 36, has daily headache for six weeks, seconds-long visual loss when she bends to pick up her child, pulsatile tinnitus, and bilateral disc swelling. CT is normal. What is the diagnosis, the next test, and the first treatment? Model: This is idiopathic intracranial hypertension until proven otherwise. Next test: MRI/MRV (exclude venous sinus thrombosis and a posterior fossa mass), then a lumbar puncture with opening pressure — elevated pressure with normal CSF (exam teaching often quotes over 25 cmH2O in adults). First treatment: weight-reduction diet plus acetazolamide (IIHTT, up to 4 g/day); serial perimetry and OCT; surgery if vision is threatened.^[6][2][23]

Stem 3 — the registrar who wants to give steroids (answer)ShowHide

A severe TBI patient has rising ICP and cerebral oedema on CT. The registrar wants to add IV dexamethasone. What is the right call, and the trial that decides it? Model: No. Corticosteroids are harmful in TBI — CRASH: 2-week mortality 21.1 vs 17.9 percent (RR 1.18); 6-month 25.7 vs 22.3 percent (RR 1.15). Reserve dexamethasone for vasogenic oedema (Ryken 4 to 8 mg/day mild, 16 mg/day or more if severe mass effect; Kostaras max 16 mg in four doses after HGG surgery). For this patient: head up 30 degrees, PaCO2 35 to 40 mmHg, mannitol 0.5 to 1 g/kg or hypertonic saline, treat the cause — no steroids.^[18][3][21]

References28ShowHide

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